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Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
Published on: April 26, 2017
A saga of cancer epigenetics: linking epigenetics to alternative splicing
Sathiya Pandi Narayanan1, Smriti Singh1, Sanjeev Shukla2
1Epigenetics and RNA Processing Laboratory (ERPL), Department of Biological Sciences, Indian Institute of Science Education and Research Bhopal (IISERB), Bhopal, Madhya Pradesh, India.
Abstract:
The discovery of an increasing number of alternative splicing events in the human genome highlighted that ∼94% of genes generate alternatively spliced transcripts that may produce different protein isoforms with diverse functions. It is now well known that several diseases are a direct and indirect consequence of aberrant splicing events in humans. In addition to the conventional mode of alternative splicing regulation by 'cis' RNA-binding sites and 'trans' RNA-binding proteins, recent literature provides enormous evidence for epigenetic regulation of alternative splicing. The epigenetic modifications may regulate alternative splicing by either influencing the transcription elongation rate of RNA polymerase II or by recruiting a specific splicing regulator via different chromatin adaptors. The epigenetic alterations and aberrant alternative splicing are known to be associated with various diseases individually, but this review discusses/highlights the latest literature on the role of epigenetic alterations in the regulation of alternative splicing and thereby cancer progression. This review also points out the need for further studies to understand the interplay between epigenetic modifications and aberrant alternative splicing in cancer progression.
Insights
Aberrant alternative splicing, a cause of disease, is increasingly regulated by epigenetic modifications. This review explores how epigenetic changes influence splicing and cancer progression, highlighting the need for further research.
Area of Science:
- Molecular Biology
- Genetics
- Epigenetics
Background:
- Alternative splicing generates diverse protein isoforms from ~94% of human genes.
- Aberrant splicing is linked to various human diseases.
- Epigenetic modifications are emerging as key regulators of alternative splicing.
Purpose of the Study:
- To review the latest literature on epigenetic regulation of alternative splicing.
- To highlight the role of epigenetic alterations in cancer progression.
- To emphasize the interplay between epigenetic modifications and aberrant splicing in cancer.
Main Methods:
- Literature review of recent studies.
- Analysis of epigenetic mechanisms influencing splicing.
- Discussion of splicing dysregulation in cancer.
Main Results:
- Epigenetic modifications regulate alternative splicing by affecting transcription elongation or recruiting splicing factors.
- Aberrant alternative splicing and epigenetic alterations are individually associated with diseases.
- Evidence suggests a significant role for epigenetics in splicing-driven cancer progression.
Conclusions:
- Epigenetic alterations play a crucial role in regulating alternative splicing.
- The interplay between epigenetic modifications and aberrant splicing is critical in cancer progression.
- Further research is needed to fully elucidate these complex interactions in cancer.
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